Microorganism populations in animal digestive systems are enormously complex biological ecosystems. Microorganisms normally inhabit the gastrointestinal tracts of human beings and other animals without invading the deeper tissues to cause disease. These microbes are consistently present in varying proportions. Their pattern of growth, conspicuously bacterial, is associated with the well-being of the animal and is necessary to its health.
Literally hundreds of species have been identified from animal intestinal tracts, and their populations can exceed 100 billion/g contents.
Typical residents of the gastrointestinal tract include coliforms, enterococci, Clostridium species, Proteus species, yeasts, Penicillium species, enteroviruses, Pseudomonas aeruginosa, aerobic and anaerobic streptococci, staphylococci, enterococci, Alcaligenes faecalis, Bacteroides species, and Lactobacillus species.
Microbial growth in the gastrointestinal tract is much more plentiful in the large intestine than the small intestine. The large intestine extends from the ileum to the anus and includes the cecum with vermiform appendix, colon, and rectum. The cecum is a blind pouch or cul-de-sac which forms the first portion of the large intestine. It is located below the entrance of the ileum at the ileocecal valve.
The age of the animal has a profound effect on intestinal physiology and microbial populations. Animals are born with a sterile intestinal tract and become colonized by those microbes in feed, or from their environment. Adult animals have a generally stable microflora that is usually disturbed only by drugs, disease, stress, or marked dietary changes.
The interaction between the animal, its environment, diet, and its residential microbial gut community is poorly understood. Inferences from the microbial balance have been made for the presence or absence of the disease state, and for reduced animal performance.
As an example, failure of chickens to reach expected levels of egg production is a problem frequently encountered in commercial egg-producing operations. Reduced egg production can be caused by a variety of viral, bacterial, toxic, and nutritional etiologies.
Commercial chickens in the United States and Europe have been reported to be infected with pathogenic intestinal spirochetes. In 1955, spirochetes were observed in cecal nodules of chickens, and these lesions were reproduced in chickens and turkeys by oral administration of infected cecal material. Mathey, W. J., et al. (1955), Spirochetes and cecal nodules in poultry. J. Am. Vet. Med. Assoc. 126:475-477. In 1986, it was reported that the isolation of a weakly hemolytic spirochete from the cecal mucosa of hens with diarrhea, chickens and swine from the same farm had a history of intermittent diarrhea. Davelaar, F. G., et al. (1986), Infectious typhlitis in chickens caused by spirochetes. Avian Pathol. 15:247-258. A subsequent fluorescent antibody microscopic study identified intestinal spirochetes in 27.6% of flocks with intestinal disorders and in 4.4% of flocks lacking signs of enteritis. Dwars, R. M., et al. (1989), Incidence of spirochetal infections in cases of intestinal disorders in chickens. Avian Pathol. 18:591-595. Retarded growth rates and delayed onset of egg production were associated with spirochete infection of pullets in Great Britain. Griffiths, I. B., et al. (1987), Retarded growth rate and delayed onset of egg production associated with spirochete infection in pullets. Vet. Rec. 121:35-37. The latter chickens were reared on deep litter and had indirect contact with swine. Further, pasty vents and dirty eggshells in Ohio laying hens shortly after molting were associated with cecal spirochetes. Swayne, D. E., et al. (1992), Association of cecal spirochetes with pasty vents and dirty eggshells in layers. Avian Dis. 36:776-781.
While the above reports indicated an association between cecal spirochetes and infection in chickens, the oral administration of human spirochetes to broiler chicks did not cause clinical signs of disease or gross lesions. Dwars, R. M., et al. (1992), Infection of broiler chicks (Gallus domesticus) with human intestinal spirochaetes. Avian Pathol. 21:559-568. However, inoculating avian intestinal spirochetes into the crop of hens resulted in wet droppings and invasion of spirochetes into and beneath cecal epithelium. Dwars, R. M., et al. (1990), Observations on avian intestinal spirochaetosis. Vet. O. 12:51-55.
In 1993, it was determined that intestinal cecal spirochetes were a cause of reduced egg production during the early part of the first laying cycle. Trampel, D. W., et al. (1994), Cecal Spirochetosis in Commercial Laying Hens. Avian Dis. 38:895-898. In this study, affected chickens necropsied were found to have an orderly, dense, uniform layer of spirochetes covering the entire mucosal surface of the ceca. Id.
Current treatments for intestinal pathogens have included treatment with therapeutic drugs, such as antimicrobials, to eradicate or decrease the number of pathogens. However, if the animal is a domesticated livestock animal used for human food consumption, adulteration of the carcass with drugs is not desirable.
Other treatments for intestinal pathogens in poultry and other livestock have included the administration of competitive exclusion products. Direct feed microbials have been successfully used to replenish the gut bacterial population with natural beneficial bacteria. One such product, sold under the trade name Preempt.RTM., contains 29 different species of bacteria. It is desirable to narrow the strains of the direct feed microbials to those minimum number of strains which are efficacious in order to decrease cost and to maximize benefit to the animal. In fact, one of the greatest difficulties with these direct feed treatments has been to find which strains from the wide consortium of bacteria, are truly effective in producing the desired result in animals, and especially livestock.
It has now been discovered that a single, defined bacterium is effective in reducing or eliminating diseases caused by undesirable microbes which colonize the ceca of animals. The bacteria corrects the pathology of the animal's system in such a manner that the host animal is quickly returned to an economically producing animal.
Accordingly, it is a primary objective of the present invention to provide a competitive exclusion product to provide a method of enhancing the overall well-being of poultry by use of a single, defined bacterium.
It is a further objective of the present invention to provide a competitive exclusion product which, when fed, corrects the pathology of the animal system in such a manner that the host animal is quickly returned to an economically producing animal.
It is another objective of the present invention to provide a competitive exclusion product in the form of a direct-fed microbial composition which can be fed in conjunction with daily free choice feed rations.
It is yet another objective of the present invention to provide a competitive exclusion product which can be fed to poultry in order to increase overall health, well being, and in general, increase the economics of the animal to its producer.
It is still a further objective of the present invention to provide a competitive exclusion product which contains only one, defined bacterium, and therefore does not contain extraneous, costly and unnecessary strains of bacteria.
It is another objective of the present invention to provide a competitive exclusion product which is safe and economical to administer to the animal.
The method and means of accomplishing each of the above objectives as well as others will become apparent from the detailed description of the invention which follows hereafter.